...
首页> 外文期刊>The FEBS journal >Interaction of HIV-1 with dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin-expressing cells is influenced by gp120 envelope modifications associated with disease progression
【24h】

Interaction of HIV-1 with dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin-expressing cells is influenced by gp120 envelope modifications associated with disease progression

机译:HIV-1与树突状细胞特异性细胞间粘附分子3的非整合素表达细胞的相互作用受与疾病进展相关的gp120包膜修饰的影响

获取原文
获取原文并翻译 | 示例
           

摘要

Dendritic cells can enhance the replication of HIV-1 in CD4(+) lymphocytes through the interaction of the gp120 envelope protein with such molecules as dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin. The variable loops of gp120 have previously been shown to modulate the interaction of HIV-1 with its principal receptor CD4 and its various coreceptors, namely CCR5 and CXCR4. Here, we utilized a panel of molecular cloned viruses to identify whether gp120 modifications can influence the virus interaction with immature dendritic cells or a cell line expressing dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (Raji-DC-SIGN). The viruses encompass the R5, R5X4 and X4 phenotypes, and are based upon V1V2 and V3 sequences from a patient with disease progression. We found that dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin enhancement of virus replication can be modulated by the V1V2 length, the overall V3 charge and N-linked glycosylation patterns; similar results were observed with immature dendritic cells. Viruses with higher V3 charges are more readily transferred to CD4(+) lymphocytes when the V1V2 region is longer and contains an additional N-linked glycosylation site, whereas transfer of viruses with lower V3 charges is greater when the V1V2 region is shorter. Viruses differing in the V1V2 and V3 regions also demonstrated differential capture by Raji-DC-SIGN cells in the presence of mannan. These results indicate that the interaction between HIV-1 and immature dendritic cells via such molecules as dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin may have a role in selecting viruses undergoing transmission and evolution during disease progression.
机译:树突状细胞可以通过gp120包膜蛋白与诸如树突状细胞特异性细胞间粘附分子3-整合素的分子相互作用来增强CD4(+)淋巴细胞中HIV-1的复制。先前已显示gp120的可变环可调节HIV-1及其主要受体CD4及其各种共受体,即CCR5和CXCR4的相互作用。在这里,我们利用一组分子克隆的病毒来鉴定gp120修饰是否可以影响病毒与未成熟树突状细胞或表达树突状细胞特异性细胞间粘附分子3-整合素(Raji-DC-SIGN)的细胞系的相互作用。该病毒涵盖R5,R5X4和X4表型,并基于疾病进展患者的V1V2和V3序列。我们发现树突状细胞特定的细胞间粘附分子3-劫持非整联蛋白增强病毒复制可以通过V1V2长度,总体V3电荷和N-联糖基化模式来调节;未成熟树突状细胞观察到相似的结果。当V1V2区域较长且包含一个额外的N-联糖基化位点时,具有较高V3电荷的病毒更容易转移至CD4(+)淋巴细胞,而当V1V2区域较短时,具有较低V3电荷的病毒的转移会更大。在甘露聚糖存在下,V1V2和V3区域中的病毒也表现出Raji-DC-SIGN细胞的差异捕获。这些结果表明,HIV-1与未成熟树突细胞之间的相互作用,例如通过树突细胞特异性细胞间粘附分子-3-捕获非整联蛋白分子,可能在选择疾病进展过程中正在传播和进化的病毒中起作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号